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Retinoic acid is an active derivative of vitamin A and regulates the differentiation, proliferation, and antimicrobial peptide expression profiles of human cells. The aim of the present study was to analyze the effect of systemic retinoic acid use on serum, saliva, and gingival tissue levels of human β-defensin (hBD)-1, hBD-2, and hBD-3.A total of sixty-nine participants (34 systemic retinoic acid users and 35 healthy controls) were enrolled in this study. Plaque index (PI), probing pocket depth (PPD), bleeding on probing (BOP), and clinical attachment loss (AL) were measured. Saliva and serum hBD-1, hBD-2, and hBD-3 levels were quantified by enzyme-linked immunosorbent assay. Gingival tissue hBD-1, hBD-2, and hBD-3 levels were determined by immunohistochemistry. Univariate general linear model was used in adjusted comparisons of hBD1, hBD-2, and hBD-3. A p value of0.05 was considered statistically significant.Reduced salivary levels of hBD-2 (p = 0.042), but not hBD-1 or hBD-3, were detected in systemic retinoic acid users compared to non-user controls. There was a significant difference in the adjusted (BOP%) salivary hBD-2 concentrations between retinoic acid and control groups (p = 0.031). No difference was observed in serum or tissue levels of hBD-1, hBD-2, or hBD-3 between two study groups.Systemic retinoic acid use associates with suppressed salivary hBD-2 level, which is independent of the gingival inflammation. This article is protected by copyright. All rights reserved.

To examine whether functional gene polymorphisms of toll-like receptor (TLR)1, TLR2, and TLR6 are related to the salivary concentrations of human beta-defensins (hBDs)-1, -2, -3, and human neutrophilic peptide (HNP)-1.Polymorphisms of TLR1 (rs5743618), TLR2 (rs5743708), and TLR6 (rs5743810) were genotyped by PCR-based pyrosequencing from the salivary samples of 230 adults. Salivary hBD-1, -2, -3, and HNP-1 concentrations were measured using enzyme-linked immunosorbent assay. General and periodontal health examinations, including panoramic radiography, were available for all participants.The genotype frequencies for wild types and variant types were as follows: 66.5% and 33.5% for TLR1, 95.5% and 4.5% for TLR2, and 25.1% and 74.9% for TLR6, respectively. The TLR2 heterozygote variant group exhibited higher salivary hBD-2 concentrations than the TLR2 wild-type group (p = .038). On the contrary, elevated hBD-2 concentrations were detected in the TLR6 wild-type group compared with the TLR6 heterozygote and homozygote variant group (p = .028). The associations between TLR6 genotypes and salivary hBD-2 concentrations remained significant after adjusting them for periodontal status, age, and smoking.hBD-2 concentrations in saliva are related to TLR2 and TLR6 polymorphisms, but only the TLR6 genotype seems to exhibit an independent association with the salivary hBD-2 concentrations.

Background: This cross-sectional study aimed to evaluate salivary concentrations of macrophage activation-related chemokines and mitogen-activated kinase kinase (MAPKK)-degrading proteolytic activity in children and adolescents with and without type 1 diabetes mellitus (T1DM). Methods: A total of 122 children and adolescents (65 T1DM patients, 50.8% female, mean age:10.9 years; 57 systemically healthy controls, 36.8% female, mean age: 9.5 years) were included in the study. Salivary concentrations of interferon gamma inducible protein-10 (IP-10), monocyte chemoattractant protein (MCP)-1, MCP-2, MCP-3, MCP-4, macrophage-derived chemokine (MDC), macrophage migration inhibitory factor (MIF), monokine induced by interferon gamma (MIG), and macrophage inflammatory protein-1 alpha (MIP-1α) were quantified using a bead-based technique. MAPKK-degrading proteolytic activity was detected using fluorescent peptide substrates. Results: The T1DM group had higher plaque index (PI%, p = 0.032) and bleeding on probing (BOP%, p = 0.045) scores, and lower decayed, missing, filled teeth (dmft/DMFT, p = 0.002) index scores compared to the healthy controls. Compared to the controls, salivary MCP-1 (p = 0.007), MCP-3 (p

ObjectiveTo monitor salivary B-cell activating factor (BAFF), tumor necrosis factor-like weak inducer of apoptosis (TWEAK), and soluble (s)CD163 levels and arginase activity in periodontitis patients following nonsurgical periodontal treatment. BackgroundBAFF, TWEAK, and sCD163 and arginase are associated with activities of B cells and macrophages, which are important regulators of periodontal immune-inflammatory response and healing following treatment. Increased salivary BAFF and sCD163 levels and arginase activity in periodontitis have been demonstrated, but their changes following treatment have not been evaluated before. Materials and MethodsForty-four Stage III/IV periodontitis patients and 35 periodontally healthy controls were included in the study. Full-mouth periodontal measurements were recorded and unstimulated saliva was obtained from all participants at baseline. Sample collection and measurements were repeated in periodontitis patients at 2, 6, 12, and 24 weeks following full-mouth scaling and root debridement, whereas controls were only seen at baseline. BAFF, TWEAK, and sCD163 levels were analyzed with bead-based multiplexed immunoassay. Arginase activity was measured with Chinard's method. ResultsBAFF (p < .001) and sCD163 (p = .003) levels and arginase activity (p < .015) were higher in periodontitis patients compared to healthy controls. BAFF levels (p < .001) and arginase activity (p < .001) of periodontitis patients were reduced at 2 weeks posttreatment and continued to decrease up to 6 (p = .038) and 12 weeks (p = .024), respectively. The reduction of sCD163 levels became significant (p = .003) at 24 weeks posttreatment. ConclusionsThe decrease in salivary BAFF levels 2 weeks after periodontal treatment indicates a change in cell signaling toward limited B-cell activation. Decreasing arginase activity similarly reflects a significant reduction in inflammatory response. The reduction in sCD163 levels that are observed at 24 weeks may reflect a longstanding anti-inflammatory macrophage activation, given their multiple functions in immune response, inflammation, and healing.

Background The aim of this study was to examine the relationship between healing response after non-surgical periodontal treatment and baseline gingival tissue levels of M2 macrophage activation-related proteins CD163, interleukin (IL)-10, interferon (IFN)-gamma, and tumor necrosis factor-like weak inducer of apoptosis (TWEAK), and the CD163/TWEAK ratio. Methods Eighty-eight gingival tissue samples from 44 Stage III/IV, Grade C periodontitis patients (18 smokers) and 41 tissue samples from 41 periodontally healthy participants (18 smokers) were evaluated. Clinical parameters were recorded in periodontally healthy individuals at baseline and in periodontitis patients at pre-treatment and 2, 6, and 12 weeks following therapy. IL-10, IFN-gamma, CD163, and TWEAK levels were analyzed with Luminex technique. Results Tissue levels (median, 1(st)-3(rd) quartile) of IL-10 (pg/ng protein), CD163 (pg/mu g protein) and TWEAK (pg/mu g protein) were as follows: IL-10 periodontitis: 2.08, 0.86-5.32 and periodontally healthy: 5.22, 3.20-10.25; CD163 periodontitis: 8.85, 4.92-14.06 and periodontally healthy: 18.36, 12.51-34.02; TWEAK periodontitis: 0.08, 0.05-0.11 and periodontally healthy: 0.16, 0.12-0.21. IL-10, CD163, and TWEAK levels were higher (P < 0.001) in periodontally healthy tissues than in periodontitis tissues. Pocket closure at 12 weeks was associated with elevated baseline gingival CD163 levels (P = 0.047) and CD163/TWEAK ratio (P = 0.001). Elevated baseline gingival CD163/TWEAK ratio was associated with pocket reduction at 6 (P = 0.022) and 12 weeks (P = 0.002). Conclusion Associations of pocket closure with pre-treatment gingival tissue CD163 levels and CD163/TWEAK ratio indicate that baseline M2 macrophage activation profile may play a role in periodontal wound healing.

The number of studies that aims to apply host- or microbe-derived biochemical biomarkers to periodontal disease diagnosis has increased significantly during the last three decades. The biochemical markers can reflect the presence, severity, and activity of periodontal diseases; however, heterogeneities in applied laboratory methods, data presentation, statistical analysis, and data interpretation prevent the translation of candidate host- or microbe-derived biochemical biomarkers to clinical assay validation. Here, we propose a roadmap for making the research outcomes comparable and re-analysable with the ultimate goal of translating research to clinical practice. This roadmap presents reporting recommendations for host- or microbe-derived biochemical biomarker studies in periodontology. We aim to make essential elements of the research work (including diagnostic criteria, clinical endpoint definitions, participant recruitment criteria, sample collection and storage techniques, biochemical and microbiological detection methods, and applied statistical analysis) visible and comparable.